Metabolic and immune pathways are extensively integrated in health and disease. Specific metabolites in the cholesterol and tricarboxylic acid (TCA) cycle have an effect on inflammation [
14,
15], and, conversely, infectious diseases in pregnancy may contribute to developmental origins of metabolic conditions [
16]. Viral infections in pregnancy, specifically by enteroviruses [
17], have been associated with type 1 diabetes in the offspring, though the mechanisms are complex and evidence circumstantial [
18,
19]. Two recent systematic reviews and meta-analyses identified a potentially causative link between maternal viral infections in pregnancy and type 1 diabetes in the offspring [
20,
21]. Interestingly, monocytes from mothers with gestational diabetes show a proinflammatory profile [
22], which can also be induced in fetal monocytes of mothers infected with hepatitis B virus [
22]. Together, these studies highlight a close relationship between hyperglycaemia and inflammatory memory [
23]. Infections in pregnancy, such as premature births with chorioamnionitis, have been associated with histone modification changes in cord-blood monocytes [
24], and inflammation memory in vitro is epigenetically modulated [
25] and reversible [
26]. These findings indicate that infection in utero can alter epigenetic patterns in offspring cells, supporting a causal link between infection and offspring obesity, mediated by metabolic and epigenetic reprogramming.